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Myocardial hypertrophy in transgenic mice overexpressing the bovine growth hormone (bGH) gene.

Fu, Michael, 1963 (author)
Gothenburg University,Göteborgs universitet,Wallenberglaboratoriet,Wallenberg Laboratory
Törnell, Jan, 1960 (author)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för kroppssammansättning och metabolism,Institute of Internal Medicine, Dept of Body Composition and Metabolism
Schulze, W (author)
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Hoebeke, Johan (author)
Gothenburg University,Göteborgs universitet,Wallenberglaboratoriet,Wallenberg Laboratory
Isaksson, Olle, 1943 (author)
Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Institute of Internal Medicine
Sandstedt, Jonas, 1966 (author)
Gothenburg University,Göteborgs universitet,Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi,Institute of Physiology and Pharmacology, Dept of Physiology
Hjalmarson, Åke, 1937 (author)
Gothenburg University,Göteborgs universitet,Wallenberglaboratoriet,Wallenberg Laboratory
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 (creator_code:org_t)
Wiley, 2000
2000
English.
In: Journal of internal medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 247:5, s. 546-52
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • OBJECTIVES: The main purpose of the present study was to characterize cardiac muscle hypertrophy using both qualitative and quantitative microscopy in mice overexpressing the bovine growth hormone. RESULTS: Measurements of 30 fibres from each group revealed that fibre diameter in transgenic hearts was significantly larger than in control hearts. There was a significant decrease in interfibrillar space in transgenic hearts as compared with control hearts. The enlarged transgenic hearts displayed unchanged organelles such as normal myofibrils and mitochondria in a normal pattern, suggesting balanced growth. Myelin structures were occasionally observed between normal myofibrils. Moreover, myocardial beta-adrenergic receptors and muscarinic receptors in the hearts of transgenic mice overproducing GH were studied to see whether they are involved in the hypertrophic process. It was shown that the density of muscarinic receptors had decreased and the super-high affinity of muscarinic receptors was lost, without any significant changes in either the density or the affinity of beta-adrenergic receptors, as compared with controls. CONCLUSIONS: These results demonstrate that a GH excess was able to induce significant myocardial hypertrophy and that there was a downregulation of muscarinic receptors.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Fysiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Physiology (hsv//eng)

Keyword

Animals
Binding
Competitive
Cardiomegaly
genetics
metabolism
Cattle
Gene Expression
Growth Hormone
genetics
metabolism
Mice
Mice
Transgenic
Microscopy
Electron
Myocardium
ultrastructure
Radioimmunoassay
Receptors
Adrenergic
beta
analysis
Receptors
Muscarinic
analysis

Publication and Content Type

ref (subject category)
art (subject category)

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